PMID- 23437123
OWN - NLM
STAT- MEDLINE
DCOM- 20130821
LR  - 20220318
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 2
DP  - 2013
TI  - Overexpression of miR -155 promotes proliferation and invasion of human laryngeal 
      squamous cell carcinoma via targeting SOCS1 and STAT3.
PG  - e56395
LID - 10.1371/journal.pone.0056395 [doi]
LID - e56395
AB  - MicroRNA155 plays an important role in many solid malignancies. Expression and 
      function of miR-155 in laryngeal carcinoma have not been fully understood. This 
      study aims to investigate the expression and function of miR-155 in laryngeal 
      squamous cell carcinoma (LSCC), the relationship between miR-155 and its 
      downstream target suppressor of cytokine signaling 1 (SOCS1)-STAT3 pathway, and 
      the related clinicopathological factors. Sixty-three samples of laryngeal 
      squamous cell carcinoma and twenty-one samples of control mucosa obtained from 
      total laryngectomy cases were analyzed using Western blot analysis and real-time 
      PCR. Hep-2 cells were cultured and transfected with miR-155 mimic and ASO. Cell 
      proliferation, migration and invasion assays were used to determine the role of 
      miR-155 in regulation of LSCC growth, migration, and invasion, respectively. The 
      expression levels of miR-155 in LSCC were significantly higher than those in the 
      control mucosa tissues. Downregulation of SOCS1 expression and elevated 
      expression of STAT3 were also observed in LSCC. The relevance of the three 
      factors were statistically significant. Moreover, knockdown of miR-155 elevated 
      SOCS1expression level, suppressed STAT3 expression, and inhibited hep-2 cells 
      growth, migration and invasion. Whereas overexpression of miR-155 inhibited 
      SOCS1expression, elevated STAT3 expression, and promoted hep-2 cells growth, 
      migration and invasion. Furthermore, the miR-155 levels in T(3) T(4) stages, and 
      poor/moderate cell differentiation were significantly higher than those in T(2) 
      stage and higher degree of cell differentiation. The STAT3 protein in 
      poor/moderate cell differentiation was significantly higher than those in higher 
      degree of cell differentiation. We firstly demonstrated the aberrant expression 
      and function of miR-155 and itsdownstream targets in LSCC. The current findings 
      suggest that miR-155 play promotingrole during the development of LSCC, and 
      miR-155 may be a useful marker for the prognosis and assessment of therapeutic 
      effects.
FAU - Zhao, Xu-dong
AU  - Zhao XD
AD  - Department of Otorhinolaryngology, Shengjing Hospital, China Medical University, 
      Shenyang, China.
FAU - Zhang, Wei
AU  - Zhang W
FAU - Liang, Hong-jun
AU  - Liang HJ
FAU - Ji, Wen-yue
AU  - Ji WY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130220
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (MIRN155 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (SOCS1 protein, human)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 0 (Suppressor of Cytokine Signaling 1 Protein)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
SB  - IM
MH  - Aged
MH  - Carcinoma, Squamous Cell/*genetics/*pathology
MH  - Case-Control Studies
MH  - Cell Movement/genetics
MH  - Cell Proliferation
MH  - Down-Regulation/genetics
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Knockdown Techniques
MH  - Humans
MH  - Laryngeal Neoplasms/*genetics/*pathology
MH  - Male
MH  - MicroRNAs/*genetics/metabolism
MH  - Middle Aged
MH  - Mucous Membrane/metabolism/pathology
MH  - Neoplasm Invasiveness
MH  - STAT3 Transcription Factor/genetics/*metabolism
MH  - Suppressor of Cytokine Signaling 1 Protein
MH  - Suppressor of Cytokine Signaling Proteins/genetics/*metabolism
MH  - Transfection
PMC - PMC3577898
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/02/26 06:00
MHDA- 2013/08/22 06:00
PMCR- 2013/02/20
CRDT- 2013/02/26 06:00
PHST- 2012/08/02 00:00 [received]
PHST- 2013/01/09 00:00 [accepted]
PHST- 2013/02/26 06:00 [entrez]
PHST- 2013/02/26 06:00 [pubmed]
PHST- 2013/08/22 06:00 [medline]
PHST- 2013/02/20 00:00 [pmc-release]
AID - PONE-D-12-23397 [pii]
AID - 10.1371/journal.pone.0056395 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(2):e56395. doi: 10.1371/journal.pone.0056395. Epub 2013 Feb 20.